Atrial fibrillation (AF) and prediabetes share common pathophysiological mechanisms with endothelial dysfunction and inflammation playing a key role. The resultant vicious cycle which sets in culminates in a higher atherogenicity and thermogenicity of the vascular system resulting in increased major adverse cardiac or cerebrovascular event (MACCE) events. However, the same has not convincingly been verified in real-world settings. In the recent retrospective study by Desai
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Batta et al. (2024) studied this question.
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